Relevant bibliographies by topics / ABCC3

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Academic literature on the topic 'ABCC3'

Author: Grafiati
Published: 10 September 2021
Last updated: 11 March 2023

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Journal articles on the topic "ABCC3"

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Leprohon, Philippe, Danielle Légaré, and Marc Ouellette. "Intracellular Localization of the ABCC Proteins of Leishmania and Their Role in Resistance to Antimonials." Antimicrobial Agents and Chemotherapy 53, no. 6 (2009): 2646–49. http://dx.doi.org/10.1128/aac.01474-08.

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ABSTRACT The ABCC subfamily of proteins is composed of nine members in Leishmania. We report that all of these proteins have an intracellular localization and that the overexpression of at least four members, ABCC3, ABCC4, ABCC5, and ABCC7, can confer resistance to antimonials, the first-line drug against Leishmania.
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Ghanem, Carolina I., and Jose E. Manautou. "Modulation of Hepatic MRP3/ABCC3 by Xenobiotics and Pathophysiological Conditions: Role in Drug Pharmacokinetics." Current Medicinal Chemistry 26, no. 7 (2019): 1185–223. http://dx.doi.org/10.2174/0929867325666180221142315.

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Liver transporters play an important role in the pharmacokinetics and disposition of pharmaceuticals, environmental contaminants, and endogenous compounds. Among them, the family of ATP-Binding Cassette (ABC) transporters is the most important due to its role in the transport of endo- and xenobiotics. The ABCC sub-family is the largest one, consisting of 13 members that include the cystic fibrosis conductance regulator (CFTR/ABCC7); the sulfonylurea receptors (SUR1/ABCC8 and SUR2/ABCC9) and the multidrug resistanceassociated proteins (MRPs). The MRP-related proteins can collectively confer resistance to natural, synthetic drugs and their conjugated metabolites, including platinum-containing compounds, folate anti-metabolites, nucleoside and nucleotide analogs, among others. MRPs can be also catalogued into "long" (MRP1/ABCC1, -2/C2, -3/C3, -6/C6, and -7/C10) and "short" (MRP4/C4, -5/C5, -8/C11, -9/C12, and -10/C13) categories. While MRP2/ABCC2 is expressed in the canalicular pole of hepatocytes, all others are located in the basolateral membrane. In this review, we summarize information from studies examining the changes in expression and regulation of the basolateral hepatic transporter MPR3/ABCC3 by xenobiotics and during various pathophysiological conditions. We also focus, primarily, on the consequences of such changes in the pharmacokinetic, pharmacodynamic and/or toxicity of different drugs of clinical use transported by MRP3.
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Norris, M. D., J. Smith, A. Kwek, et al. "Expression of the multidrug transporter genes ABCC1/MRP1, ABCC3/MRP3, and ABCC4/MRP4 are powerful predictors of clinical outcome in childhood neuroblastoma." Journal of Clinical Oncology 25, no. 18_suppl (2007): 9524. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.9524.

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9524 Background: We have previously shown, both retrospectively and prospectively, that high-level expression of the multidrug transporter gene ABCC1/MRP1, is strongly predictive of poor outcome in the childhood cancer neuroblastoma (NEJM, 334:231–8, 1996; JCO, 24:1546–53, 2006), and that ABCC1/MRP1 can be regulated by the MYCN oncogene. The contribution of other ABCC family genes to clinical outcome in this disease has now been examined. Methods: Real-time quantitative PCR was used to determine ABCC gene expression in a large prospectively accrued cohort (n=209) of primary untreated neuroblastomas from patients enrolled on POG biology protocol 9047. Results: Older age, advanced stage, and MYCN amplification were all predictive of poor outcome in the cohort. Amongst the ABCC family, high levels of ABCC1 and ABCC4, but low levels of ABCC3, were strongly associated with reduced survival and event-free survival (P<0.005) in the overall study population, and also in subgroups of patients lacking MYCN amplification. Following adjustment for the effect of MYCN gene amplification and other prognostic indicators by multivariate analysis, expression of ABCC1 (HR=2.3; p=0.03), ABCC3 (HR=2.7; p=0.0141), ABCC4 (HR=3.4; p=0.002) retained significant prognostic value for outcome, whereas age and MYCN amplification lost all prognostic significance. By combining the expression of these three transporter genes, patients could be stratified into groups having excellent, intermediate or poor outcome (EFS=84%, 59%, 17%, respectively). Conclusions: These data, suggest that ABCC1, 3 and 4 are amongst the most powerful prognostic markers yet identified for childhood neuroblastoma and as such represent important targets for potential therapeutic intervention. No significant financial relationships to disclose.
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Malinowski, Damian, Paweł Grzegółkowski, Katarzyna Piotrowska, Marcin Słojewski, and Marek Droździk. "Membrane Transporters and Carriers in Human Seminal Vesicles." Journal of Clinical Medicine 11, no. 8 (2022): 2213. http://dx.doi.org/10.3390/jcm11082213.

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Seminal vesicles play an important role in the male reproductive system, producing seminal fluid and thus adequate environment for sperm. However, mechanisms underlying secretory functions of the seminal vesicles’ epithelium have not been defined yet. The aim of the present study was to characterize expression and immunolocalization of selected membrane transporters and carriers in the seminal vesicles. The study included biopsy specimens collected from non-affected parts of seminal vesicles from 53 patients of Caucasian origin subjected for prostatectomy. RT-PCR was used to define expression of 15 genes coding for ABC-family and 37 genes encoding 37 SLC-family transporters/carriers. Immunohistochemistry was used to define localization of 6 transporters. In the seminal vesicles, the following membrane transporters and carriers were defined: ABCA1, ABCB1, ABCB5, ABCB6, ABCC1, ABCC2, ABCC3, ABCC4, ABCC5, ABCC6, ABCG2, SLC01C1, SLC02B1, SLC04A1, SLC04C1, SLC10A1, SLC15A1, SLC15A2, SLC16A1, SLC16A3, SLC19A1, SLC22A1, SLC22A3, SLC22A11, SLC22A18, SLC22A4, SLC22A5, SLC28A1, SLC2A9, SLC33A1, SLC47A1, SLC47A2, SLC51A, SLC51B, SLC7A5, SLC7A6. Age-dependent expression was evidenced for ABCB1, ABCG2, SLC04C1, SLC15A1, SLC16A1, SLC22A11, SLC22A18, SLC47A1 and SLC47A2. ABCG2, P-gp, MRP1, MRP3, MCT1 and LAT1 were localized in the apical membrane and P-gp in the basolateral membrane of the seminal vesicle epithelium. The expression of the membrane transporters and carriers in the seminal vesicle epithelium confirms its secretory and barrier functions.
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Encarnación-Medina, Jarline, Rosa I. Rodríguez-Cotto, Joseph Bloom-Oquendo, Mario G. Ortiz-Martínez, Jorge Duconge, and Braulio Jiménez-Vélez. "Selective ATP-Binding Cassette Subfamily C Gene Expression and Proinflammatory Mediators Released by BEAS-2B after PM2.5, Budesonide, and Cotreated Exposures." Mediators of Inflammation 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/6827194.

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ATP-binding cassette subfamily C (ABCC) genes code for phase III metabolism proteins that translocate xenobiotic (e.g., particulate matter 2.5 (PM2.5)) and drug metabolites outside the cells. IL-6 secretion is related with the activation of the ABCC transporters. This study assesses ABCC1–4 gene expression changes and proinflammatory cytokine (IL-6, IL-8) release in human bronchial epithelial cells (BEAS-2B) exposed to PM2.5 organic extract, budesonide (BUD, used to control inflammation in asthmatic patients), and a cotreatment (Co-T: PM2.5 and BUD). A real-time PCR assay shows that ABCC1 was upregulated in BEAS-2B exposed after 6 and 7 hr to PM2.5 extract or BUD but downregulated after 6 hr of the Co-T. ABCC3 was downregulated after 6 hr of BUD and upregulated after 6 hr of the Co-T exposures. ABCC4 was upregulated after 5 hr of PM2.5 extract, BUD, and the Co-T exposures. The cytokine assay revealed an increase in IL-6 release by BEAS-2B exposed after 5 hr to PM2.5 extract, BUD, and the Co-T. At 7 hr, the Co-T decreases IL-6 release and IL-8 at 6 hr. In conclusion, the cotreatment showed an opposite effect on exposed BEAS-2B as compared with BUD. The results suggest an interference of the BUD therapeutic potential by PM2.5.
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Falasca, Marco, Xi Chen, and Gary Piazza. "Abstract 1814: Novel ABC transport inhibitor as a treatment for pancreatic and prostate cancers." Cancer Research 82, no. 12_Supplement (2022): 1814. http://dx.doi.org/10.1158/1538-7445.am2022-1814.

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Abstract ABC transporters are the active transport systems of the cell involved in the export or import of a wide variety of molecules. We discovered that a member of the ABC transporter family called ABCC3 has a critical role in pancreatic cancer. ABCC3 blockade using genetic knockdown inhibits pancreatic cancer growth in vitro and in vivo. In addition, we demonstrate that knockdown of ABCC3 reduces cell proliferation by inhibition of STAT3 and HIF1α signalling pathways, which are key regulators of pancreatic cancer progression. A focused chemical library of indenes was screened for ABCC3 inhibition using ABCC3 expressing pancreatic tumour cells. A drug development candidate, designated as S3, emerged following extensive chemical modification to optimize target selectivity and oral bioavailability. Oral administration of S3 significantly inhibited tumour growth and increased survival in several mouse models of pancreatic cancer without discernible toxicity. Interestingly, using the KPC transgenic mouse model that closely mimics human pancreatic cancer, we identified a dual activity of S3 to inhibit the growth of the primary tumour and impact the surrounding stroma. Strikingly, a significant increase in survival was achieved with S3 treatment compared to vehicle treated KPC mice. A two-fold increase in lifespan was observed from 72.5 days (median survival) in the control group to 146.5 days in the treatment group. Importantly, we observed no overt toxicity from S3 treatment at a dosage of 50 mg/kg, which generated plasma levels exceeding growth inhibitory IC50 values. Furthermore, we show that stromal cells in pancreatic tumours, which actively participate in cancer progression, are enriched for ABCC3, and that its inhibition may contribute to stroma reprogramming. In other studies, we found that S3 inhibits the closely related transporter, ABCC1, and that pharmacological inhibition of ABCC1 reduced prostate cancer cell growth in vitro and potentiated the effects of Docetaxel in vitro and in mouse models of prostate cancer in vivo. Mechanistically, we have shown that ABCC3, is overexpressed in pancreatic cancer cells and can efflux the bioactive lipid lysophosphatidylinositol (LPI) which, in turn, activates its receptor G protein-coupled receptor 55 in an autocrine mitogenic loop. Similarly, ABCC1 mediates LPI efflux in prostate cancer cells. The fact that both ABCC1 and ABCC3 transport LPI and are inhibited by S3 is not surprising considering that they share a high primary sequence identity and are known to have overlapping substrate specificity. Interestingly, unlike known ABC inhibitors, S3 has anticancer activity as a single agent. Our goal is to further study the antitumor activity of S3 alone and in combination with conventional chemotherapy or molecular targeted drugs used for the treatment of pancreatic and prostate cancer. Citation Format: Marco Falasca, Xi Chen, Gary Piazza. Novel ABC transport inhibitor as a treatment for pancreatic and prostate cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1814.
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Leprohon, Philippe, Danielle Légaré, Isabelle Girard, Barbara Papadopoulou, and Marc Ouellette. "Modulation of Leishmania ABC Protein Gene Expression through Life Stages and among Drug-Resistant Parasites." Eukaryotic Cell 5, no. 10 (2006): 1713–25. http://dx.doi.org/10.1128/ec.00152-06.

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ABSTRACT The ATP-binding cassette (ABC) protein superfamily is one of the largest evolutionarily conserved families and is found in all kingdoms of life. The recent completion of the Leishmania genome sequence allowed us to analyze and classify its encoded ABC proteins. The complete sequence predicts a data set of 42 open reading frames (ORFs) coding for proteins belonging to the ABC superfamily, with representative members of every major subfamily (from ABCA to ABCH) commonly found in eukaryotes. Comparative analysis showed that the same ABC data set is found between Leishmania major and Leishmania infantum and that some orthologues are found in the genome of the related parasites Trypanosoma brucei and Trypanosoma cruzi. Customized DNA microarrays were made to assess ABC gene expression profiling throughout the two main Leishmania life stages. Two ABC genes (ABCA3 and ABCG3) are preferentially expressed in the amastigote stage, whereas one ABC gene (ABCF3) is more abundantly expressed in promastigotes. Microarray-based expression profiling experiments also revealed that three ABC genes (ABCA3, ABCC3, and ABCH1) are overexpressed in two independent antimony-resistant strains compared to the parental sensitive strain. All microarray results were confirmed by real-time reverse transcription-PCR assays. The present study provides a thorough phylogenic classification of the Leishmania ABC proteins and sets the basis for further functional studies on this important class of proteins.
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Iraci, Nunzio, Simona Soverini, Samuele Gherardi, et al. "Expression Profiling of ABC Transporter Genes in Chronic Myeloid Leukemia (CML) and Responsiveness to Imatinib." Blood 112, no. 11 (2008): 3193. http://dx.doi.org/10.1182/blood.v112.11.3193.3193.

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Abstract The deregulation of ATP-binding cassette (ABC) transporters responsible for the efflux of anticancer agents may involve mutations or single nucleotide polymorphisms (SNPs) or an increase in their expression level. Consequently, chemoresistance may develop. We have previously shown that the expression level and transcription of ABC drug transporters in CML cells is affected by c-Myc. Our results demonstrated that c-Myc is highly expressed in CD34+ cells from newly diagnosed chronic phase (CP)-CML patients, and that it can significantly upregulate the expression of several ABC genes, particularly, the ABCC1, ABCC4 and ABCG2, while it downregulates the expression of ABCC3. We have also demonstrated that c-Myc was a direct regulator and physically associated with the promoter of tested ABC genes, as assessed by Chromatin Immunoprecipitation in a cell line derived from a Ph+ CML patient. Taken together, our findings supported the model of a direct and coordinate regulation of a large set of ABC genes by the c-Myc transcription factor. Our study also supported prior findings that deregulation of specific set of ABC genes could be an important molecular mechanism altering imatinib transport. Based on these observations we have started to investigate the role of ABC transport genes expression in newly diagnosed CP-CML patients treated with imatinib. RNA extracted from white blood cells of 5 patients who achieved a stable major molecular response (MMR) by 12 months (responders) and 15 patients who didn’t show a partial cytogenetic response (CgR) by 6 months nor a complete CgR by 12 months (suboptimal responders according to European LeukemiaNet recommendations). All pts were enrolled on GIMEMA CML Working Party-sponsored clinical trials of imatinib. A panel of ABC genes including ABCB1, ABCB9, ABCC1, ABCC3, ABCC4, ABCE1 and ABCG2 was interrogated by Q-PCR for the level of expression. Results were normalized to the expression of three reference genes, i.e., GUSB, b-actin and GAPDH. Our results show that suboptimal responders display high expression levels of ABCG2 (p<0.01) and very low levels of ABCC3 (p<0.0001) as compared to patients with responders. Interestingly, when ABC expression profile of the same patient was evaluated before starting imatinib treatment and compared with a measurement obtained at the time of suboptimal response, we could not observe any significant difference between the two conditions. That suggest that this specific ABC transporter expression profile could be present at diagnosis. Although preliminary, our findings suggest that profiling of ABC drug transporter genes in CML patients could provide a novel modality of investigating their responsiveness to imatinib. Analysis of a larger series of patients is ongoing to further explore the potential predictive value of this expression profile. We speculate that ABCC3, which is strongly repressed possibly through a typical epigenetic mechanisms such as promoter hypermethylation and/or chromatin condensation, could be re-activated by means of demethylating agents or inhibitors of chromatin condensation. Thus, our study proposes that an important novel approach to optimize imatinib response in such patients merits further investigations.
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Mutch, David M., Pascale Anderle, Muriel Fiaux, et al. "Regional variations in ABC transporter expression along the mouse intestinal tract." Physiological Genomics 17, no. 1 (2004): 11–20. http://dx.doi.org/10.1152/physiolgenomics.00150.2003.

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The ATP-binding cassette (ABC) family of proteins comprise a group of membrane transporters involved in the transport of a wide variety of compounds, such as xenobiotics, vitamins, lipids, amino acids, and carbohydrates. Determining their regional expression patterns along the intestinal tract will further characterize their transport functions in the gut. The mRNA expression levels of murine ABC transporters in the duodenum, jejunum, ileum, and colon were examined using the Affymetrix MuU74v2 GeneChip set. Eight ABC transporters (Abcb2, Abcb3, Abcb9, Abcc3, Abcc6, Abcd1, Abcg5, and Abcg8) displayed significant differential gene expression along the intestinal tract, as determined by two statistical models (a global error assessment model and a classic ANOVA, both with a P < 0.01). Concordance with semiquantitative real-time PCR was high. Analyzing the promoters of the differentially expressed ABC transporters did not identify common transcriptional motifs between family members or with other genes; however, the expression profile for Abcb9 was highly correlated with fibulin-1, and both genes share a common complex promoter model involving the NFκB, zinc binding protein factor (ZBPF), GC-box factors SP1/GC (SP1F), and early growth response factor (EGRF) transcription binding motifs. The cellular location of another of the differentially expressed ABC transporters, Abcc3, was examined by immunohistochemistry. Staining revealed that the protein is consistently expressed in the basolateral compartment of enterocytes along the anterior-posterior axis of the intestine. Furthermore, the intensity of the staining pattern is concordant with the expression profile. This agrees with previous findings in which the mRNA, protein, and transport function of Abcc3 were increased in the rat distal intestine. These data reveal regional differences in gene expression profiles along the intestinal tract and demonstrate that a complete understanding of intestinal ABC transporter function can only be achieved by examining the physiologically distinct regions of the gut.
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Franz, Laura, Klaus Raming, and Ralf Nauen. "Recombinant Expression of ABCC2 Variants Confirms the Importance of Mutations in Extracellular Loop 4 for Cry1F Resistance in Fall Armyworm." Toxins 14, no. 2 (2022): 157. http://dx.doi.org/10.3390/toxins14020157.

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Fall armyworm (FAW), Spodoptera frugiperda, is a highly destructive and invasive global noctuid pest. Its control is based on insecticide applications and Bacillus thuringiensis (Bt) insecticidal Cry toxins expressed in transgenic crops, such as Cry1F in Bt corn. Continuous selection pressure has resulted in populations that are resistant to Bt corn, particularly in Brazil. FAW resistance to Cry1F was recently shown to be conferred by mutations of ATP-binding cassette transporter C2 (ABCC2), but several mutations, particularly indels in extracellular loop 4 (ECL4), are not yet functionally validated. We addressed this knowledge gap by baculovirus-free insect cell expression of ABCC2 variants (and ABCC3) by electroporation technology and tested their response to Cry1F, Cry1A.105 and Cry1Ab. We employed a SYTOXTM orange cell viability test measuring ABCC2-mediated Bt toxin pore formation. In total, we tested seven different FAW ABCC2 variants mutated in ECL4, two mutants modified in nucleotide binding domain (NBD) 2, including a deletion mutant lacking NBD2, and S. frugiperda ABCC3. All tested ECL4 mutations conferred high resistance to Cry1F, but much less to Cry1A.105 and Cry1Ab, whereas mutations in NBD2 hardly affected Bt toxin activity. Our study confirms the importance of indels in ECL4 for Cry1F resistance in S. frugiperda ABCC2.
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Dissertations / Theses on the topic "ABCC3"

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Wang, Zhan. "IMPACT OF MULTIDRUG RESISTANCE-ASSOCIATED PROTEIN 2 (MRP2/ABCC2) AND 3 (MRP3/ABCC3) ON THE PHARMACOKINETICS OF METHOTREXATE." Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/179025.

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Pharmaceutical Sciences<br>Ph.D.<br>This dissertation presents an investigation of the impact of Multidrug Resistance-associated Protein 2/ATP-binding cassette superfamily C member 2 (Mrp2/Abcc2) and 3 (Mrp3/Abcc3) on the pharmacokinetics (PKs) of methotrexate (MTX) using gene knockout murine models. MTX is a substrate for numerous human ATP-binding cassette (ABC) efflux transporters, yet the impact of these transporters on the pharmacokinetics of MTX over a large dose range has not been examined. To investigate the effects of two transporters, Abcc2 (Mrp2) and Abcc3 (Mrp3), involved in MTX hepatobiliary disposition in vivo, MTX plasma, urine and feces concentrations were analyzed after 10, 50, and 200 mg/kg intravenous (IV) doses to groups of wild type (WT), Abcc2-/- and Abcc3-/- mice. The absence of Abcc2 caused a decrease in total clearance of MTX relative to WT mice at all dose levels yet was accompanied by compensatory increases in renal excretion and metabolism to 7-hydroxymethotrexate (7OH-MTX). In Abcc3-/- mice total clearance was elevated at the two lower dose levels that was attributed to stimulation of biliary excretion and confirmed by elevated fecal excretion; however at the high 200 mg/kg dose clearance was severely retarded and could be attributed to hepatotoxicity as conversion to 7OH-MTX was diminished. We also sought to characterize the effects of Abcc2 and Abcc3, on the PKs of MTX after oral dosing. Plasma, urine, and fecal concentrations of MTX were measured after 10, 50, and 200 mg/kg oral doses to cohorts of WT, Abcc2-/- and Abcc3-/- mice mouse strains. The absence of Abcc2 caused an approximate 2-fold increase in system exposure and a slight increase in oral bioavailability of MTX relative to WT mice at all dose levels. These elevations were accompanied by compensatory increases in conversion to 7OH-MTX, and based on AUC7OH-MTX/AUCMTX (area under the curve ratio of metabolite and parent drug) that ranged from 3% to 9% in WT mice increased to a range of 16% to 26% in Abcc2-/- mice. Renal excretion of unchanged MTX was unaltered in the Abcc2-/- strain; fraction urinary excretion (fr) ranged from about 4% to 11% in WT mice, whereas in Abcc2-/- mice fr ranged from about 7% to 23%. Abcc3-/- mice exhibited more than a 2-fold decrease in Cmax and significant reductions in AUCMTX when compared to WT mice at all dose levels. There were no compensatory increases in either metabolism or in renal and biliary excretion, which suggests future studies for investigating a potential unknown mechanism. Regardless of the mouse strain, increases in the MTX dose were not accompanied by proportional increases in AUCMTX. The PKs of MTX in different mouse strains was successfully modeled by a nonlinear semi-mechanistic 3-compartmental conditional model incorporating key efflux transporters. The model employed population-based analysis and conditional transport terms to well capture the nonlinear properties of MTX systemic disposition for a wide dose range of 10 - 200 mg/kg in WT and knockout strains. The model correlates the mechanistic nature of the nonlinear phenomenon with the key efflux transporters effects on MTX PKs and provides insight for preclinical therapeutic study design. Overall, the information obtained in this investigation underscores the significance of efflux transporters, Abcc2 and Abcc3, for they significantly influence the pharmacokinetics of MTX and their impact can be reflected by a nonlinear semi-mechanistic 3-compartmental conditional model. The studies also provide implication in the preclinical therapeutic study design and insights on the source of inter-patient variability as well as on the combination drug regimens to maximize drug activity yet without toxicity.<br>Temple University--Theses
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PESSINA, SARA. "The multidrug-resistance transporter Abcc3 protects NK cells from chemotherapy in a murine model of malignant glioma." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/94457.

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Il glioblastoma (GBM) è la forma più frequente ed aggressiva dei tumori cerebrali. Le opzioni terapeutiche convenzionali sono attualmente rappresentate da resezione chirurgica della massa tumorale seguita da radioterapia e chemioterapia con temozolomide (TMZ). Nonostante l’uso di strategie terapeutiche aggressive, la prognosi complessiva resta infausta. L’immunoterapia, descritta nel 2013 “breakthrough dell’anno” da Science, è il principale avanzamento nel GBM. Di particolare interesse è la valutazione degli effetti della chemioterapia in combinazione con l’immunoterapia. La chemioterapia, storicamente considerata immunosoppressiva, può avere effetti stimolatori sul sistema immunitario. In uno studio clinico attualmente attivo presso il nostro istituto, pazienti con prima diagnosi di GBM in seguito a intervento chirurgico e dopo leucaferesi ricevono un trattamento standard di radioterapia e chemioterapia con temozolomide (RT-TMZ) e TMZ come adiuvante in combinazione con vaccinazioni con cellule dendritiche. Una caratterizzazione del sistema immunitario è condotta su sangue periferico dei pazienti con particolare attenzione alla risposta effettrice citotossica. L’aumento della risposta delle cellule NK ma non dei linfociti T CD8+ è al momento correlato significativamente con una prolungata sopravvivenza. Per cercare di comprendere un potenziale effetto diretto della TMZ sulle cellule immuni abbiamo sfruttato un modello murino di glioma maligno focalizzandoci sulla caratterizzazione dei meccanismi molecolari indotti dalla TMZ sui linfociti. Nel nostro studio, topi con glioma GL261 sono stati trattati con cinque iniezioni intraperitoneali di TMZ 9 giorni dopo l'impianto intracranico del tumore. La TMZ ha indotto una rapida e reversibile linfopenia di linfociti T CD8+. Al contrario, la frequenza delle cellule NK è aumentata rapidamente già dopo la seconda somministrazione del farmaco. Le analisi del profilo di espressione genica sui linfociti del sangue periferico ha rivelato un’up-regolazione di Abcc3, trasportatore associato a farmacoresistenza, nelle NK ma non nei linfociti T CD8+ durante il trattamento. Abcc3 si è rivelato funzionalmente attivo e necessario per la sopravvivenza delle cellule NK. Infatti solo le cellule NK non esprimenti Abcc3 sono sensibili alla TMZ e per questo più inclini ad entrare in apoptosi. L’inattivazione farmacologica di Abcc3 ha inoltre indotto un aumento significativo di apoptosi confermando il suo ruolo cruciale nella resistenza delle cellule NK alla TMZ. Durante il trattamento l’attivazione di Akt, proteina chiave per la sopravvivenza, è stata individuata solo in cellule NK esprimenti Abcc3 e non nei linfociti T CD8+, i quali hanno mostrato un significativo aumento di apoptosi. La resistenza delle cellule NK è associata ad un aumento della loro capacità migratoria con conseguente maggior infiltrato nei gliomi dei topi trattati con TMZ. Le cellule NK inoltre infiltrano il tumore precocemente determinando un aumento persistente delle molecole citotossiche quali IFN-γ, granzimi e perforina. Abbiamo inoltre evidenziato che la profonda modulazione del microambiente tumorale indotta dalla TMZ fornisce la condizione ottimale per l'infiltrazione e l’attività citotossica delle cellule NK. La citotossicità delle cellule NK nel sangue, valutata come produzione di IFN-γ e capacità litica delle cellule GL261, aumenta significativamente. I nostri dati mostrano, per la prima volta, che Abcc3 è cruciale nel conferire alle cellule NK resistenza alla chemioterapia. La TMZ inoltre è in grado di promuovere l’attivazione di meccanismi responsabili della sopravvivenza delle cellule NK e della loro risposta anti-tumorale. Queste osservazioni hanno una importante ripercussione clinica e potrebbero avere implicazioni per i pazienti affetti da GBM e trattati con chemio-immunoterapia.<br>Glioblastoma (GBM) is the most common and aggressive form of malignant brain tumors. The current standard treatments for GBM patients still consist of surgical resection of the tumor mass followed by radiotherapy and chemotherapy with temozolomide (TMZ). In spite of therapeutic progresses, the patient prognosis is poor and the recurrence very frequent. There is an urgent need of novel therapeutic strategies in order to prevent or realistically to delay the recurrence. Cancer immunotherapy, the scientific breakthrough of year 2013 by Science, is the main progress in cancer therapy. A growing amount of preclinical and clinical studies unravels the possibility to potentiate the immune system against GBM. A number of data show that several anticancer agents, including classical chemotherapeutic compounds previously viewed as immunosuppressive, are able to enforce tumor specific immune responses when in combination with immunotherapy. In a clinical trial currently active at our institute, patients with first diagnosis of GBM after surgery and leukapheresis receive standard treatment with radio-chemotherapy with temozolomide (RT-TMZ) and TMZ as adjuvant during DC vaccines. Peripheral blood lymphocytes (PBLs) are analyzed by flow cytometry to characterize immune response with special interest to CD8+ T lymphocytes and Natural Killer (NK) cells, which are responsible of effector response. A significant increase and activation of peripheral blood NK cells, but not CD8+ T cells, correlates significantly with a prolonged survival of patients. In order to evaluate a potential direct effect of TMZ on immune system, we focused our study on the molecular mechanisms induced by TMZ on immune cells in a murine model of malignant glioma. We treated GL261 glioma-bearing mice with five intraperitoneal injections of TMZ 9 days after intracranial tumor implantation. TMZ induced a rapid and reversible decrease of CD8+ T cell frequency. Otherwise, trafficking and homing of NK cells rapidly increased after the second TMZ administration. Gene expression profiling on PBLs revealed an up-regulation of the multidrug-resistance protein Abcc3 in NK cells, but not in CD8+T cells, from TMZ-treated compared to mice treated with vehicle as control. We found that Abcc3 is functionally active during chemotherapy treatment and intrinsically required for NK cell survival. Only Abcc3 negative NK cells are more prone to undergo apoptosis. The pharmacological inactivation of Abcc3 induced a significant increase of apoptosis in NK cells demonstrating its crucial role in inducing NK cell resistance to TMZ. Akt activation, key of survival pathways, was found only in NK cells that express Abcc3 and not detected in CD8+ T cells that showed a remarkable increase in apoptosis during TMZ treatment. Moreover, the resistance of NK cells to TMZ was accompanied by increased migration and homing into the brain at early time points. NK cells infiltrate the tumor mass early leading to an increase and persistent expression of cytotoxic signals including IFN-γ, granzymes and perforin. Additionally, the profound modulation of glioma microenvironment induced by TMZ provided the optimal condition for NK cell infiltration and cytotoxic function. Cytotoxicity, evaluated as IFN-γ production and specific lytic activity against GL261 cells by peripheral NK cells, significantly increased compared to control mice. Our data showed, for the first time, that Abcc3 expression confers NK cell resistance to chemotherapy. Furthermore, TMZ influenced NK cell functions promoting mechanism involved in cell survival and in the specific anti-tumor response. These observations have clinical implications for GBM patients treated with chemo-immunotherapy.
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Zehnpfennig, Britta. "Modellsysteme für humanes ABCC3 : Funktionelle Rekonstitution und Charakterisierung in Proteoliposomen und Aufbau biosensorischer Oberflächen /." Münster, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000252269.

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Chan, Yuen Man. "Functional analysis of single nucleotide polymorphisms in the proximal promoter regions of the multidrug transporter genes MRP1/ABCC1 and MRP4/ABCC4." Thesis, Kingston, Ont. : [s.n.], 2007. http://hdl.handle.net/1974/730.

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Thajam, Deirdre. "The role of multidrug resistance proteins in determining fetal susceptibility to drugs of misuse." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-multidrug-resistance-proteins-in-determining-fetal-susceptibility-to-drugs-of-misuse(85fef852-5e19-4700-950e-753d85fad88c).html.

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Background: Negative outcomes from fetal exposure to maternal dug use include Neonatal Abstinence Syndrome (NAS) and altered development, the unpredictability of which suggests a biological element as yet not accounted for. The manner in which the human placenta protects the fetus from xenobiotics such as drugs of misuse is not completely characterised. However, Adenosine Triphosphate Binding Cassette (ABC) transporters in placentae have demonstrated their ability to efflux xenobiotics away from the fetal vascular compartment leading to lower concentrations than in the maternal compartment and some commonly used drugs have been shown to be substrates for these proteins, e.g. methadone. It is suggested that polymorphisms in the genes that encode these transporter proteins may alter their expression and/or function. Hypothesis- Polymorphisms (SNPs) in the ABC transporters ABCB1, ABCG2, ABCC1 and ABCC2 change protein expression and/or function leading to increased fetal exposure demonstrated by increased signs of NAS and/or altered development. Objectives: To determine if genotype alters protein expression and whether there is a relationship between the level of placental multidrug resistance protein P-glycoprotein (P-gp), Breast Cancer Resistance Protein (BCRP), Multidrug Resistance Associated Proteins (MRP1 and MRP2) expression and neonatal and/or developmental outcomes. Methods: Drug using women were recruited. In the immediate postnatal period placental tissue, cord blood and maternal hair samples were taken. Hair was analysed to determine drug use in the preceding 3 months, immunoblotting determined the level of P-gp, BCRP, MRP1 and MRP2 protein expression. Sequenom MassExtend Array produced genotypes from DNA obtained from cord blood. Infants were assessed for NAS at birth, 3 days and 3 weeks. At 8 months and 1 year development was assessed using the Griffiths Mental Development Scales. Plink was used to determine statistically significant associations between genotype and outcome phenotypes. Results- The level of fetal drug exposure did not predict the need for pharmacological treatment for NAS. 32 polymorphisms with significant associations to outcome measures were identified: 4 SNPs significantly altered protein expression, (3 for P-gp and 1 for MRP1). 41 SNPs were associated with changes across 4 of the 5 GMDS subscales. Discussion: No clear relationship between MDRP protein expression and neonatal outcome was noted. However, fetal genotype did influence the expression of P-gp and MRP1 and genotype across all four proteins was associated with significant changes in the measures of infant development. This was a small study and as such generation of susceptible haplotypes was not possible. However the data generated do support the concept. Further larger and longer term prospective studies, building on the experience reported in this thesis, are necessary to generate more data in order to identify haplotypes leading to increased fetal susceptibility to drug exposure.
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Meyer, zu Schwabedissen Henriette Elisabeth Ulrike. "Expression und Lokalisation der Eliminationstransporter ABCB1, ABCG2, ABCC2 und ABCC5 in Plazenta Einfluss von Gestationsalter, genetischen Polymorphismen und zellulärer Differenzierung ; Proteomanalyse zur Charakterisierung der In-vitro-Differenzierung isolierter Trophoblasten /." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972753427.

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Zhang, Anja Ziwen. "Sumoylierung und Targeting von ABCA3." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-146702.

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Huppmann, Marceline. "Lungenmechanische Charakterisierung von heterozygoten ABCA3-Knockout-Mäusen." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-133099.

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Lächelt, Sandra [Verfasser]. "Funktionelle Analyse von ABCC2-Haplotypen / Sandra Lächelt." Kiel : Universitätsbibliothek Kiel, 2009. http://d-nb.info/1019869933/34.

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Rodrigues, Lucas Campos de Sá. "Estudo da expressão dos genes de resistência a múltiplas drogas ABCB1, ABCC1 e ABCG2, em cães com linfoma multicêntrico, submetidos a três diferentes protocolos de tratamento antineoplásico." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-08102012-141346/.

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Um dos principais desafios no tratamento quimioterápico em seres humanos e animais é a resistência que as células neoplásicas apresentam, sendo esse mecanismo responsável por falhas no tratamento e recidivas da doença. A resistência pode ser intrínseca ou adquirida e ocorre em função da expressão de transportadores de membrana ABC, como a glicoproteína P (ABCB1/MDR), proteínas de resistência a múltiplas drogas (ABCC1/MRP) e proteína de resistência do câncer de mama (ABCG2/BCRP). O linfoma é a neoplasia hematopoiética mais comum em cães, altamente responsiva à quimioterapia, mas que recidiva durante o tratamento antineoplásico, sendo a resistência das células neoplásicas aos quimioterápicos um fator responsável pela alta taxa de recidiva e óbito dos animais. Neste estudo avaliou-se a expressão de genes relacionados à resistência a múltiplas drogas em cães com linfoma, no diagnóstico e na recidiva da doença, em três diferentes protocolos quimioterápicos utilizados na rotina clínica. A expressão dos genes ABCB1, ABCC1, ACBG2 foi determinada por RT-PCR (PCR em tempo real) em 25 animais naturalmente acometidos pela doença, divididos aleatoriamente em 3 grupos tratados com os protocolos quimioterápicos COP, VCM e Short-Madison, além de um &quot;pool&quot; controle constituído por linfonodos normais de oito animais. A expressão dos genes foi detectada em todas as amostras, tanto de linfonodos normais quanto de animais com linfoma. No diagnóstico da doença, a expressão do gene ABCC1 foi relacionada negativamente com idade (p=0,008) e positivamente com duração da remissão (p=0,027) e sobrevida (p=0,007), entretanto para os genes ABCB1 e ABCG2 não houve diferença estatística significante. Na recidiva, a expressão dos genes não sofreu variação estatística significante em função do tipo e duração da remissão e sobrevida. Não houve variação na expressão dos genes ABCB1, ACBC1 e ABCG2 no momento da recidiva quando comparado ao protocolo quimioterápico utilizado.<br>One of the main challenges of the chemotherapy treatment in human and animals is the resistance of the neoplasic cells, being this mechanism responsible for failures in the treatment and relapse of the disease. The resistance could be intrinsic or acquired and it occurs due to the expression of ABC membrane transporters, such as p-glycoprotein (ABCB1/MDR), resistance protein to multiple drugs (ABCC1/MRP) and resistance protein of breast cancer (ABCG2/BCRP). Lymphoma is the most common hematopoietic cancer disease in dogs, highly responsive to chemotherapy, but relapse during chemotherapy treatment, being the resistance of neoplastic cells to chemotherapy drugs the responsible factor for the high rate of relapse and death of animals. In this study, genes expression related to multiples drugs resistance it was evaluated in dogs with lymphoma, in the diagnosis and in the relapse of the disease in three different chemotherapy protocols used in the clinical routine. The genes expression ABCB1, ABCC1, ACBG2 was determined by RT-PCR (real time PCR) in 25 animals naturally undertaken by the illness, randomly divided into 3 groups treated with the chemotherapy protocols COP, VCM and Short-Madison, besides a &quot;pool&quot; control constituted by normal lymph node of eight animals. The genes expression was detected in all the samples, both in the normal lymph node and in the animals with lymphoma. In the diagnosis of the disease, the gene expression ABCC1 was negatively related with age (p=0,008) and positively with the duration of remission (p=0,027) and survival (p=0,007); however, for ABCB1 and ABCG2 there was no statiscally significant difference. In the relapse, the genes expression had no statiscally significant difference due to the type and duration of remission and survival. There was no variation in the genes expression ABCB1, ACBC1 and ABCG2 in the moment of relapse when compared to the chemotherapy protocol used.
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Books on the topic "ABCC3"

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Association of British Chambers of Commerce., ed. Chambers of commerce and industry in membership of the Association of British Chambers of Commerce (ABCC), 15th August 1988. ABCC, 1988.

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Association of British Chambers of Commerce., ed. Chambers of commerce and industry in membership of the Association of British Chambers of Commerce (ABCC), 7th July 1988. ABCC, 1989.

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Hull, Sarah, and Andrew R. Webster. Ophthalmic Manifestations of Inherited Metabolic Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0075.

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Systemic metabolic disorders can manifest in the cornea, lens, or retina with or without affecting vision. In some conditions findings are present from birth, and in others ophthalmic complications develop as the disease progresses. In some conditions in adults (for instance pseudoxanthoma elasticum (PXE), Wilson disease, Fabry and gyrate atrophy) ocular findings are pathognomic and should lead to targeted investigations such as sequencing of ABCC6 in PXE and serum ornithine levels in gyrate atrophy. Early diagnosis and treatment may improve visual outcomes. This chapter will focus on the key conditions in adults that have distinct presentations in the eye.
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artsy, nesto. Traceable Letters Worksheets Abc3: Letter Tracing Practice and Coloring Book, Preschool Writing Workbook ,Homeschool Preschool Learning Activities ,Kindergarten and Kids Ages 3-5. Independently Published, 2020.

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Book chapters on the topic "ABCC3"

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Nies, Anne T. "MRP2 (ABCC2) and MRP3 (ABCC3)." In Pharmacogenomics of Human Drug Transporters. John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118353240.ch15.

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Paolini, Alessandro, Antonella Baldassarre, and Andrea Masotti. "ABCA3." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101533.

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Paolini, Alessandro, Antonella Baldassarre, and Andrea Masotti. "ABCA3." In Encyclopedia of Signaling Molecules. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101533-1.

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Ford, Robert C. "ABCC7/CFTR." In ABC Transporters - 40 Years on. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-23476-2_13.

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Cheepala, Satish B., Mugdha Sukthankar, and John D. Schuetz. "MRP4 (ABCC4)." In Pharmacogenomics of Human Drug Transporters. John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118353240.ch16.

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Franco, Rodrigo, and Laura Zavala-Flores. "ABCC Transporters." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-27841-9_7076-2.

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Franco, Rodrigo, and Laura Zavala-Flores. "ABCC Transporters." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-662-46875-3_7076.

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Wada, Morimasa, Takeshi Uchiumi, and Michihiko Kuwano. "Canalicular multispecific organic anion transporter ABCC2." In Membrane Transporter Diseases. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9023-5_18.

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Nogee, Lawrence M. "Surfactant Deficiency Disorders: SP-B and ABCA3." In Molecular Basis of Pulmonary Disease. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-384-4_11.

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Weedon, Michael N., and Peter Light. "From Association to Function: KCNJ11 and ABCC8." In The Genetics of Type 2 Diabetes and Related Traits. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-01574-3_17.

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Conference papers on the topic "ABCC3"

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Pellegatta, Serena, Sara Pessina, Gabriele Cantini, Emanuela Cazzato, Dimos Kapetis, and Gaetano Finocchiaro. "Abstract 1343: Abcc3 up-regulation confers protection from chemotherapy to NK cells in a murine model of malignant glioma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1343.

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Yu, Zhiqi, Chang Zhang, Xianhua Gao, et al. "Abstract B35: Aberrant expression of ABCC3 in rectal cancer predicts poor prognosis and pathological response to neoadjuvant chemoradiotherapy via activating the caspase-3 dependent apoptotic pathway." In Abstracts: Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; Oct 27-30, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1940-6215.prev-13-b35.

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Xu, K., D. J. Wegner, H. B. Heins, P. Yang, F. S. Cole, and J. A. Wambach. "Characterization of Preferential ABCA3 Allele Expression from Lung Explants of Infants and Children with ABCA3 Deficiency." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3451.

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Si, X. C., and M. Tracy. "Not All ABCA3 Mutations Are Created Equal." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5030.

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Şişmanlar Eyuboglu, Tuğba, Tugba Ramaslı Gursoy, Ayse Tana Aslan, Zeynep Reyhan Onay, Sevgi Pekcan, and Matthias Griese. "Progressive lung disease caused by ABCA3 mutation." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3527.

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Li, Yang, Susanna Kinting, Stefanie Hoeppner, and Matthias Griese. "Functional analysis of ABCA3 in phosphatidylcholine metabolism." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3661.

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López, María Del Carmen, Estela Pérez Ruiz, Antonio Moreno Galdo, et al. "ABCA3 deficiency in a newborn with respiratory failure." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4169.

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Kinting, Susanna, Stefanie Höppner, Thomas Wittmann, et al. "Rescue of mutant ABCA3 by small molecular correctors." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa913.

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Parton, L. A., M. Scharbach, M. Leong, S. Rajbhandari, D. Kronn, and A. Banquet. "Two Novel Variants of ABCA3 Associated with BPD." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3314.

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Wittmann, Thomas, Ulrike Schindlbeck, Stefanie Höppner, et al. "Classification of different ABCA3 mutations causing interstitial lung disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4851.

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